Effects of L-arginine-derived nitric oxide synthesis on cardiovascular responses to stimulus-evoked somatosympathetic reflexes in the gracile nucleus
Effects of L-arginine-derived nitric oxide synthesis on cardiovascular responses to stimulus-evoked somatosympathetic reflexes in the gracile nucleus
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DOI：
10.1016/s0006-8993(02)03664-8
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发表时间：
2002-12-27
期刊：
影响因子：
2.9
通讯作者：
Ma, SX
中科院分区：
文献类型：
--
作者：
Chen, S;Ma, SX
这些研究的目的是确定纤薄核 (Gr) 的作用以及细胞核中 L-精氨酸衍生的一氧化氮 (NO) 合成对心血管对体交感神经反射 (SSR) 反应的影响。在麻醉的 Sprague-Dawley 大鼠中进行腓肠神经和胫神经的电刺激以引起兴奋性和抑制性 SSR。将药物显微注射到 Gr 中后，在刺激诱发的 SSR 期间监测动脉血压和心率。通过向 Gr 中微量注射利多卡因来阻断心脏对腓肠神经和胫神经电刺激的 aSCUIar 反应。通过双侧显微注射 L-精氨酸到 Gr 中，减弱了对腓肠神经刺激的高血压和心动过速反应。但由于该区域中 nNOS 反义寡脱氧核苷酸 (oligos) 的存在而增强。将 L-精氨酸显微注射到 Gr 中促进了对胫神经刺激的低血压和心动过缓反应，而用 nNOS 反义寡核苷酸预处理到 Gr 中则减弱了胫骨刺激引起的抑制性 SSR。将 nNOS 正义寡核苷酸显微注射到 Gr 中并没有改变刺激诱发的反应。结果表明，心血管对刺激诱发的 SSR 的反应因 Gr 中神经元传导的阻滞而受到抑制。 Gr 中 L-精氨酸衍生的 NO 合成减弱了心血管对刺激诱发的兴奋性 SSR 的反应，并促进了对抑制性 SSR 的反应。我们得出结论，Gr 中的 NO 通过 SSR 调节在中枢心血管控制中发挥抑制作用。 (C) 2002 Elsevier Science B.V. 保留所有权利。
The purpose of these studies was to determine the role of gracile nucleus (Gr) and the effects of L-arginine-derived nitric oxide (NO) synthesis in the nucleus on the cardiovascular responses to somatosympathetic reflexes (SSR). Electrical stimulation of sural and tibial nerve to evoke excitatory and inhibitory SSR was carried out in anesthetized Sprague-Dawley rats. Arterial blood pressure and heart rate were monitored during stimulus-evoked SSR following microinjections of the agents into Gr. Cardio aSCUIar responses to electrical stimulation of the sural and tibial nerves were blocked by microinjection of lidocaine into Gr. The hypertensive and tachycardiac responses to stimulation of the sural nerve were attenuated by bilateral microinjection of L-arginine into Gr. but enhanced by the presence of nNOS antisense oligodeoxynucleotides (oligos) in the area. Microinjection of L-arginine into Gr facilitated the hypotensive and bradycardic responses to stimulation of the tibial nerve while pretreatment with nNOS antisense oligos into Gr attenuated the tibial stimulation evoked inhibitory SSR. The stimulus-evoked responses were not altered by microinjection of nNOS sense oligos into Gr. The results show that the cardiovascular responses to stimulus-evoked SSR were inhibited by the presence of a blockade of neuronal conduction in the Gr. L-Arginine-derived NO synthesis in the Gr attenuates the cardiovascular responses to stimulus-evoked excitatory SSR and facilitates the responses to inhibitory SSR. We conclude that NO in the Gr plays an inhibitory role in the central cardiovascular control through SSR regulation. (C) 2002 Elsevier Science B.V. All rights reserved.